Radon-Induced Radiation Biomarkers: A Scoping Review from Exposure Dosimetry to Early Biological Effects on the Lung - review

Sep 22, 2026

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Radon-222, a naturally occurring radioactive gas, is a major contributor to lung cancer after tobacco. Inhalation delivers alpha-particle radiation from decay products (notably polonium-218 and polonium-214), producing dense DNA damage in bronchial epithelium. Because ambient radon measurements fluctuate widely, they often cannot determine individual internal dose. This scoping review synthesizes radon-linked biomarker strategies spanning internal dosimetry, molecular and cytogenetic damage indicators, and early biological effect markers, and assesses their feasibility in real-world occupational and residential contexts, including how smoking complicates causal interpretation through overlapping mutation pathways.

LanguageEnglish

CategoryResearch & Report

FormatPDF

Pages39

Reading Time1 h 38 min

AccessFree to download

Abstract

Keywords

1. Introduction

Review Radon-Induced Radiation Biomarkers: A Scoping Review from Exposure Dosimetry to Early Biological Effects on the Lung Phoka C. Rathebe * and Mota Kholopo Academic Editor: Maria Paola Bertuccio Received: 8 December 2025 Revised: 15 January 2026 Accepted: 16 January 2026 Published: 14 May 2026 Copyright: © 2026 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license. Department of Environmental Health, Faculty of Health Sciences, Doornfontein Campus, University of Johannesburg, P.O. Box 524, Johannesburg 2006, South Africa; [motaliok@gmail.com](motaliok@gmail.com) * [Correspondence: prathebe@uj.ac.za](Correspondence: prathebe@uj.ac.za); Tel.: +27-11-559-6641 Abstract Radon-222, a naturally occurring radioactive gas, is the second leading cause of lung cancer globally, after tobacco use. When inhaled, its decay products, especially polonium-218 and polonium-214, emit high-energy alpha particles that induce dense DNA damage in the bronchial epithelium. Because ambient radon measurements often vary significantly over time and across locations, they provide limited insight into individual exposure levels. This suggests the urgent need for biological markers that can accurately indicate internal dose and early signs of lung cancer development. This review offers an extensive overview of biomarkers associated with radon exposure, from internal dosimetry to early biological responses. It covers internal dose markers (e.g., radon progeny in air and 210Po/210Pb in bones and teeth), molecular and cytogenetic indicators of effective dose (such as chromosomal aberrations, γ-H2AX foci, and DNA adducts), and early effect markers (including somatic mutations, epigenetic changes, miRNA profiles, and autoantibody signatures) . The review highlights translocations detected via FISH, discussing those that are stable over time versus those that are transient. It also evaluates the reliability and practicality of these biomarkers in occupational and residential settings, noting how smoking complicates causal inference due to overlapping mutation pathways. Finally, it suggests that integrating multi-omics technologies could improve the precision of biomarker panels. Keywords: radon-222; alpha particles; biomarkers; miRNA; lung cancer 1. Introduction Radon-222 is a colorless, odorless radioactive gas produced by the natural decay of uranium in soil and rock. It has become a significant environmental carcinogen with widespread effects on global public health. Humans mainly encounter radon through inhalation, especially indoors, where it can build up to dangerous levels. Although it occurs naturally, radon is a subtle and often overlooked hazard, now acknowledged worldwide asthe second leading cause of lung cancer after tobacco use and the top cause among neversmokers. Recent epidemiological data highlights the significant role of radon in the global lung cancer burden. A 2022 global assessment by Shan et al. [1] estimated that lung cancer deaths due to residential radon exposure amounted to around 1.03 per 100,000 people, accounting for approximately 84,000 deaths annually worldwide. These numbers reveal a troubling ongoing impact of radon-related health issues, especially in areas with high radon levels and limited mitigation infrastructure. In the United States, the Environmental Protection Agency (EPA) estimates that about 21,000 lung cancer deaths each year are caused by radon exposure [2] . This figure surpasses other commonly discussed hazards like secondhand smoke, drunk driving, or fire-related fatalities. Notably, many of these deaths happen among people who have never smoked, highlighting radon’s ability to act as a powerful and independent carcinogen. The World Health Organization (WHO) has repeatedly highlighted these issues, stressing that radon-related lung cancers are preve

FAQs

Why are radon measurements alone often insufficient for estimating individual exposure?

Ambient radon levels vary significantly over time and across locations, so measurements may not accurately reflect a person’s internal dose.

What biological damage pathways do radon decay products trigger in the lung?

Inhaled radon decay products emit high-energy alpha particles that induce dense DNA damage in bronchial epithelium.

What types of biomarkers are covered in the review?

The review covers internal dose markers, molecular and cytogenetic indicators of effective dose, and early effect markers such as mutations, epigenetic changes, miRNA profiles, and autoantibody signatures.

Sep 22, 2026

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